- the anti-aging brain booster
by James South MA
one of the original antiaging, neuro-energizing drugs. It has been
studied and used clinically for over 50 years.
Centrophenoxine is a compound of
two chemicals, dimethylaminoethanol (DMAE) and parachlorophenoxyacetate
(pCPA). Dimethylaminoethanol is a natural food component, found especially
in fish, and is also a natural metabolite of the human body.
Centrophenoxine's other half, pCPA, is a synthetic compound similar to a variety
of plant hormones called "auxins."
Centrophenoxine – Lipofuscin
One of the earliest discoveries
from animal studies showed that centrophenoxine is extremely effective at
reducing lipofuscin levels. Lipofuscin is a "garbage residue"
biochemical conglomerate that accumulates over a lifetime, sometimes reaching
30% of the cell volume in aged animals.
As cells accumulate ever more
lipofuscin they become ever less functional, and they may die rapidly when a
critical threshold of lipofuscin accumulation is reached.
Animal studies have shown
centrophenoxine to be highly efficient at removing this cellular garbage-
notable reductions in mice occur within 6 weeks. One study with aged rats found
a 28-42% reduction in brain lipofuscin levels after 8 weeks of centrophenoxine
Both human and animal studies
have shown that low lipofuscin levels correlate with healthy cellular function,
while high lipofuscin accompanies poor cellular health.
Through a variety of animal
experiments measuring learning abilities and memory, aged animals whose high
lipofuscin levels were reduced by centrophenoxine, also had their memory and
learning abilities restored to a level similar to healthy young animals, while
untreated high lipofuscin control animals did not.
Centrophenoxine – Cognition
The chief component of
centrophenoxine is DMAE which is part of the choline betaine cycle, natural to
human and animal cells.
By adding a methyl group (CH3) to
DMAE, choline (also called trimethylaminoethanol) is formed. The choline thus
formed may then be used to make other valuable biochemicals, such as the major
neurotransmitter acetylcholine, or the essential membrane constituents
phosphatidylcholine and sphingomyelin.
Choline can also be oxidized to
make betaine (trimethylglcine), important for ridding the body of heart and
artery toxic homocysteine, now considered one of the most important risk factors
for heart disease.
Under fasting conditions, normal
blood levels of choline range from 8 to 12 micromoles. When blood choline levels
are below 14 micromoles, choline flows from brain cells into the bloodstream.
When blood choline levels are above 14 micromoles, choline flows from the blood
into the brain.
Unfortunately, when choline
enters the blood from brain cells, it is derived from auto-cannibalization, the
choline containing phospholipids (which are critical brain cell membrane
components) are broken down to provide the choline entering the blood.
There is evidence that excessive
neuronal choline auto-cannibalization over a lifetime may contribute to
Centrophenoxine – The need for
While a natural foods diet, such
as liver, meat and eggs provides high dietary levels of choline, the modern
processed junk food/ synthetic diet provides little choline, as do vegetarian
Simple choline supplements, such
as choline chloride or bitartrate are often broken down, as much as 60%, by gut
bacteria. Thus, centrophenoxine derived DMAE is an especially ideal source of
blood and brain choline for several reasons.
Gut bacteria do not digest DMAE,
thus avoiding that wasteful trap. The liver quickly and easily converts DMAE to
choline as needed. Also, DMAE prevents choline from being irreversibly oxidized
to betaine, further raising blood choline levels. Lastly, DMAE passes through
the blood brain barrier far more easily than choline.
DMAE may be incorporated into
brain cell membranes, where it functions as a powerful hydroxyl free radical
scavenger. Or the brain cells may convert the DMAE to choline for their needs.
With the help of an enzyme called "CAT", choline is converted to the
learning/ memory neurotransmitter acetylcholine.
With aging, and even more so with
Alzheimer's disease, cholinergic neurons tend to under produce acetylcholine.
Fortunately, the popular brain nutrient acetyl L-carnitine that powerfully
increases CAT activity, thus increasing acetylcholine production.
The research of Dr. Raymond
Bartus has shown that the original nootropic drug- piracetam works much more
effectively to enhance learning and memory when combined with a cholinergic
Thus, centrophenoxine, piracetam
and acetyl-L-carnitine would be an "all star" combination for
cognition enhancement. Human studies have found centrophenoxine to be
effective at restoring intellectual well being.
Centrophenoxine – The human
One study with 76 healthy
elderly, who suffered from significant intellectual deterioration, found that
centrophenoxine increased storage of new information into long term memory,
while also increasing vigilance and alertness, after only several weeks of
A double blind placebo controlled
study found clinical improvement from CPX in 7 out of 30 patients with senile
Centrophenoxine – Much more
Centrophenoxine, which is more
than just DMAE, also has a general activating effect on brain function.
Centrophenoxine enhances neuronal glucose (the chief brain fuel) and oxygen
uptake, while increasing carbon dioxide production, all signs of increased brain
Centrophenoxine also increases
neuronal RNA and protein production. RNA (derived from DNA in the cell nucleus)
"instructs" neurons how to form proteins which help encode memory, as
well as repair cell damage.
Yet brain RNA and protein
production normally drop with age, and especially when large lipofuscin deposits
form around the cell nucleus, one of the main sites where lipofuscin accumulates
in old age.
Centrophenoxine reverses this
age-related drop. It is interesting to note here that the pCPA component of CPX
is similar to plant auxins- plant hormones, which increase RNA and protein
production in growing plants.
Centrophenoxine has been shown to
increase repair of the synapses that connect nerve cells to each other- while
untreated aging synapses tend to deteriorate in number, structure and function.
Thus, because of the unique plant
auxin like substance pCPA that is combined with DMAE to make centrophenoxine,
centrophenoxine may be considered the ultimate "DMAE plus."
Centrophenoxine – the dosages
In spite of the generally
beneficent anti-aging, brain energizing, repairing effects of centrophenoxine, a
few words of caution are necessary.
Centrophenoxine is a powerful
enhancer of brain and peripheral nervous system acetylcholine levels, and too
much acetylcholine can cause problems. Excessive acetylcholine levels can lead
to headaches, neck, jaw and shoulder muscle tension, insomnia, irritability and
hyper excitability, agitation and restlessness.
If any of these occur, simply
discontinue centrophenoxine for a few days and then try a reduced dosage. Also,
those with major depression, mania, seizure disorders or Parkinson's disease
should avoid centrophenoxine, as too much acetylcholine may worsen these
conditions. Also, pregnant women should avoid centrophenoxine.
While elderly people with
significant intellectual decline/ loss of vigor may need 3 to 6 centrophenoxine
tablets per day (250mg each), taken preferably with breakfast and lunch, in
order to avoid insomnia.
For healthy younger people simply
wishing the brain protection/ cognitive boost/ choline benefits that
centrophenoxine provides may need only 1 or 2 centrophenoxine tablets (250mg
each) daily with breakfast or lunch.
To avoid any slight acetylcholine
excess that may slowly creep up unnoticed, it may be helpful to skip
centrophenoxine one or two days weekly.
Centrophenoxine: Effects on aging mammalian brain
J. AM. GERIATR. SOC. (USA), 1978, 26/2 (74-81)
A study was made of the effects of centrophenoxine on the learning and
memory of old mice. The results were correlated with changes in neuronal
lipofuscin in the cerebral cortex and hippocampus. Old female mice (11-12
months) were treated with centrophenoxine for three months and their learning
and memory were tested in a T-maze. The number of trials required to attain the
criterion in the 20 treated old mice were compared with those for 20 untreated
mice of the same age and for 20 younger untreated mice. The treated animals
learned the task with significantly fewer trials, and also exhibited a reduction
of neuronal lipofuscin pigment in both the cerebral cortex and the hippocampus.
The changes in lipofuscin were demonstrated by study of the characteristic
autofluorescence, and by histochemical and ultrastructural (electron microscope)